A perusal of the bulk of 1,489 articles published on Takotsubo syndrome (TTS) (as of December 1, 2012) suggested that this disorder is not of ischemic, but of neuromechanical, nature. “Neuro” in the sense that it is triggered by a surge in catecholamines, primarily epinephrine, and “mechanical” in the sense that its consequence is a cardiomyocyte-based hypokinesis, akinesis, or dyskinesis of the cardiac apical and medial myocardium and hyperkinesis of the cardiac base. In reference to the basal hyperkinesis, the range of its severity is large, from a state of being absent to the extreme of being very intense, resulting in marked midventricular pressure gradients. This variation could result from altered expression of the disease or the clinical presentation of patients after widely different intervals from the inception of TTS. Thus, it is conceivable that what transpires over time in terms of these regional myocardial wall contraction abnormalities is much different than what we are witnessing after the patients come to our attention. Accordingly, one wonders whether the degree of the basal hyperkinesis is greater, less, or the same as that detected at the first left ventricular angiographic or echocardiographic interrogation that patients with TTS undergo. Another matter still unexplored is whether the basal hyperkinesis is in response (compensatory) to the apical-medial hypokinesis, akinesis, or dyskinesis, modeled after the hyperkinesis or hypertrophy of the noninfarcted myocardium after large acute myocardial infarction, a “part and parcel” of the disease, or even the cause of the apical or medial “ballooning” in TTS. It is important in the elucidation of the pathogenesis of TTS and its pharmacologic or device-based therapeutic management to investigate the role that basal hyperkinesis exerts in the natural course of TTS. One could theorize that all clinical and laboratory manifestations of TTS (i.e., chest pain, dyspnea, arrhythmias, microcirculation impairment, leukocyte infiltration, myocardial-band necrosis, myocardial edema, ST-segment elevation, prolongation of the QTc interval, midventricular pressure gradients, myocardial rupture, ventricular thrombus) are totally or partially due to the systolic mechanical “stretching” of the medial-apical myocardium engendered by the basal hyperkinesis. Even if eventually the “epinephrine hypothesis” is proved correct, and it becomes accepted that that is at the root of apical-medial “ballooning,” with basal hyperkinesis being compensatory and norepinephrine-mediated, exploration of the basal hyperkinesis per se, its effect on the apical-medial mechanical “stretching” and its consequences on the myocardium would have been worthwhile. Clinically, elucidation of the role and natural course of basal hyperkinesis in patients presenting with TTS can be facilitated by expeditious and repeated application of echocardiography during hospitalization. However, this might not suffice, and an animal model of basal outflow obstruction, without the confounding effect of the catecholamine surge encountered in TTS, might be needed to evaluate the consequences of basal hyperkinesis on the “unprepared” (unlike the setting of hypertension, aortic stenosis, and hypertrophic cardiomyopathy) apical-medial myocardium. Accordingly, the following animal model is proposed: a catheter with a cylindrical balloon inserted by way of the carotid or femoral artery and positioned and stabilized using a guidewire in the subaortic region in adult anesthetized rats, will be employed. The catheter will provide continuous aortic and left ventricular blood pressure monitoring by way of the aortic and ventricular apical ports. A baseline echocardiogram will be recorded in the parasternal long-axis view and a 12-lead electrocardiogram will be recorded. Blood will be drawn for baseline creatine kinase, MB-creatine kinase, and cardiac troponin I measurement. An apparatus will be used for an electrocardiogram QRS-triggered inflation of the balloon after an appropriate electromechanical delay. Such inflations will ensure that the aortic blood pressure will be adequate, although some hypotension, not unlike that experienced by patients with TTS, is advisable. Periodic monitoring of the electrocardiogram, echocardiogram, and myocardial biomarkers will be done. Finally, necropsy with full gross anatomic, histologic, histochemical, electron microscopic assessment, and evaluation for water content of cardiac tissues from the base, midventricle, and apex of the studied rats will be performed.